Abstract
The in vivo reducing ability of a nitroxide radical, 4-hydroxyl-2,2,6,6-tetramethylpiperidin-1-oxyl (TEMPOL), in the liver of rats was estimated by using an electron spin resonance spectrometer equipped with a surface-coil-type resonator following administration of glucose. Both oral and intravenous administration of glucose significantly enhanced the reduction capacity. In vitro studies show that the reduction site of TEMPOL in the hepatic homogenate is located in the mitochondrial respiratory chain and microsomal electron transport system. These findings indicate that the enhancement of activity of these systems caused by the glucose administration prompts reduction of TEMPOL in the liver.
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